Ch. 4 Cardiovascular Function Flashcards Preview

Pathophysiology > Ch. 4 Cardiovascular Function > Flashcards

Flashcards in Ch. 4 Cardiovascular Function Deck (67):

what are the functions of the cardiovascular system?

deliver vital oxygen and nutrients to the cells, removes waste products, and transports hormones


how does the lymphatic system assist in maintaining homeostasis?

by returning excess fluid from the body's tissues back to the circulatory system as well as by playing a vital role in the immune system


how does the pericardium protect the heart?

protects it against trauma from surrounding structures, invasions of foreign bodies, and friction from the constant movement. it also provides support in terms of anchoring the heart and prevents over distention



process by which cardiac cells are able to generate an impulse to contract even with no external nerve stimulus


the SA node automatically generates impulses at what rate?

60-100 bpm


the AV node is able to initiate impulses at what rate?

40-60 bpm


what can happen if the impulses fail to fire at the SA or AV nodes?

the ventricles will attempt to pace themselves, but can only generate impulses around 20-40 bpm, which may not result in adequate cardiac output because the ventricles may not have a chance to fill completely before they contract


what does the P wave on an EKG represent?

atrial contraction or depolarization


on an EKG what does the QRS complex represent?

ventricular contraction or depolarization. atrial reploarization occurs here, but we don't see it because it is masked by the ventricular depolarization


what does a more intense contraction do to the EKG?

it creates a higher wave or complex


what does the T wave represent on an EKG?

ventricular repolarization or relaxation


abnormal variations in the EKG

arrhythmias or dysrhythmias


what ions do the cardiac muscle cells need in order to work? why?

Na, K, and Ca. need Na and K for the sodium-potassium pumps that will initiate and conduct electrical signals. need Ca for muscle contractility. need Na for the neurologic system which controls the cardiac function


how does the nervous system function in the contractility of the heart?

rate of contraction (chronotropic effect), rate of electrical conduction (dromotropic effect), and strength of the contraction (inotropic effect)


detect chemical changes in the blood



located in the carotid artery. detect the pressure in the heart and arteries



what will stimulating the SNS do to the heart rate and blood pressure? what about the parasympathetic nervous system?

SNS will increase heart rate and blood pressure, parasympathetic will decrease heart rate and blood pressure


what is pulse pressure?

the difference between the systolic and diastolic pressures and represents the force that the heart generates each time it contracts


what two things significantly affect blood pressure? what is the equation?

cardiac output and peripheral vascular resistance


the force opposing blood in the peripheral circulation. it increases as the diameter of the blood vessel decreases. stimulation of the SNS can initiate systemic vasoconstriction to raise blood pressure

peripheral vascular resistance


how does the afterload affect the heart?

the higher the afterload, the harder it is for the heart to eject blood, thus lowering the stroke volume


how is the stroke volume affected by preload?

the amount of blood returning to the heart that the heart must then manage


what happens as afterload and preload increase?

blood pressure increases


how does antidiuretic hormone affect blood pressure and volume?

it increases water reabsorption in the kidney, so increases the blood volume and pressure. additionally it is a vasoconstrictor which increases the PVR, which also increases blood pressure


how does aldosterone affect blood volume and pressure?

it increases blood volume by increasing the reabsorption of Na in the kidneys which attracts water. increasing renal water reabsorption will increase blood volume and pressure


how does the renin-angiotensin-aldosterone system affect the heart?

becomes activated when renal blood flow decreases. stimulates aldosterone secretion. in hypotensive states, this mechanism raises blood pressure and maintains the blood supply to vital organs


what happens to the renin-angiotensin-aldosterone system in chronic disease states such as hypertension?

it is inappropriately activated because of vasoconstriction to the kidneys and further contributes to hypertension


what are the three layers in the walls of blood vessels?

tunica intima - smooth, thin, inner layer
tunica media - middle layer composed of elastic tissue and smooth muscle responsible for the vessels ability to change diameter
tunica externa/adventitia - outer layer that consists of elastic tissue and fibrous connective tissue to provide the necessary give to accommodate the rush of blood with each cardiac contraction


what are the lymphatic organs and what is their primary function?

lymph nodes, spleen, thymus, and tonsils. they primarily function in immune response


normally, the rate at what lymph is produced equals what?

the rate at which it is removed, but in some body states, the amount produced exceeds the capacity of the system


decreased cardiac output can be associated by changes in what things?

preload, afterload, contractility, or dysrhythmias


what do the manifestations of decreased cardiac output reflect?

typically reflect the inability to meet the body's needs and may include fatigue, oliguria, cyanosis, fluid accumulation, and decreased peripheral pulses


a state in which there is a decrease in nutrition and oxygenation at the cellular level due to a deficit in capillary blood flow supply

altered tissue perfusion


what can altered tissue perfusion be associated with?

an interruption of blood flow, decreased cellular exchange, and fluid shifts


what do the typical manifestations of altered tissue perfusion reflect?

cellular ischemia and may include pain, skin changes, and signs of organ necrosis


an inflammation of the pericardium. because of this inflammation fluid shifts from the capillaries into the pericardial cavity between the sac and the heart



what are the different types of fluid that may fill the pericardial cavity in pericarditis?

serous resulting from heart failure, purulent resulting from infections, serosanguineous resulting from neoplasms or uremia, hemorrhagic resulting from aneurysms or trauma


pericarditis causes fluid to accumulate in the cavity which may lead to a pericardial effusion. the pericardial effusion can then lead to a cardiac tamponade. what is a cardiac tamponade?

fluid accumulates in the pericardial cavity to the point that it compresses the heart. the heart cannot fill and stretch during diastole, resulting in decreased cardiac output. eventually heart fialure, cardiogenic shock, and death can result


what are the manifestations of a cardiac tamponade?

arterial pressures fall, venous pressures rise, and pulse pressure narrows due to the decreased stretch of the heart. heart sounds are muffled upon auscultation because the fluid in the cavity drowns out the sound


what is constrictive pericarditis?

the pericardium becomes thick and fibrous from chronic inflammation and adheres to the heart. there is a loss of elasticity which restricts the cardiac filling, decreasing cardiac output and causing systemic congestion


what are the clinical manifestations of pericarditis?

pericardial friction rub; sharp, sudden, severe chest pain that increases with deep inspiration and is relieved when the person sits up and leans forward; dyspnea; tachycardia; edema; flu-like symptoms; restlessness; irritability; anxiety; friction rub may be auscultated


what is the cause of acute pericarditis?

a lot of times it is unknown but it can be caused by a viral infection


what are risk factors for pericarditis?

heart surgery, uremia, heart attack, some autoimmune conditions


infection of the endocardium, the inner layer of the heart, or the valves

infective endocarditis


what are the most common causes of infective endocarditis?

Streptococcus viridans commonly found in the mouth account for 50% of all cases, Staphylococcus aureaus and S. enterocuccus which are commonly found on the skin also are frequent causative agents


what occurs during infective endocarditis?

endothelial damage attracts platelets and stimulates thrombus formation. vegetation collects on the internal structures because of damage from the infection. with each heart contraction, some of this vegetation is dislodged and ejected from the heart. these small thrombi move throughout the body and collect in the small vessels and create microhemorrhages. the valves can become scarred and perforated.


if untreated how does infective endocarditis usually end?

it usually turns out to be fatal, especially when it involves the valvular structures


what are the risk factors for the development of infective endocarditis?

intravenous drug use, valvular disorders, prosthetic heart valves, rheumatic heart disease, coarctation of the aorta, congenital heart defects, Marfan syndrome


what are the clinical manifestations of infective endocarditis?

flulike symptoms, embolization, new onset of heart murmur or change in a heart murmur that was already present, petechiae, splinter hemorrhages under the nails, hematuria, Olser's nodes, fever


tender, raised, subcutaneous lesions on the fingers and toes

Olser's nodes


what is done to prevent infectious endocarditis in certain patients?

patients who are deemed at risk are given special antibiotics before surgery and procedures that protect them against their increased risk. dental surgeries are a big one


these cause disruption of normal blood flow through the heart and can be either stenosis or regurgitatoin

valvular disorders


narrowing of a tubular structure



what occurs when the heart valves are stenosed?

blood backs up in the chamber just before the valve. pressure in the overfilled chambers increased to pump against the resistance of the stenosed valve. hypertrophy of the chambers develops and this plus the increased work load increases the oxygen demands of the heart tissue, but because of the decreased cardiac output, it is harder to meed those demands. without adequate blood flow, the heart deteriorates


occurs when the valve leaflets do not completely close



what does the regurgitation of blood do to the heart?

increases the amount of blood that must be pumped and in turn the cardiac workload. this contributes to hypertrophy in the affected chambers. the increased blood volume in the heart causes the chambers to dilate to accommodate the blood volume


what are some causes of valvular disorders?

congenital defects, infective endocarditis, rheumatic fever, hypertension, myocardial infarction, cardiomyopathy, heart failure


how is the heart affected during an aortic stenosis?

blood flow is affected from the left ventricle into the aorta during systole. left ventricle is having to work harder to push the blood into the aorta


how is the heart affected by a mitral stenosis?

blood flow is impaired from left atria into left ventricle. left atrium is having to work harder to get blood into the ventricle


backflow of blood into the left ventricle during diastole

aortic regurgitation


back flow of blood into the left atrium during systole

mitral valve regurgitation


back flow of blood into the right atrium during systole

tricuspid regurgitation


ballooning or billowing upwards of the leaflets of the mitral valve when the ventricles contract

mitral valve prolapse. if it worsens it can lead to mitral valve regurgitation


group of conditions that weaken and enlarge the myocardium



what are the risk factors for developing dilated cardiomyopathy?

increased age, African American men, chemotherapy, alcoholism, cocaine and amphetamine abuse, pregnancy, infections, thyrotoxicosis, diabetes mellitus, neuromuscular disorders, hypertension, coronary artery disease, hypersensitivity to medications. most cases are idiopathic, but these things can increase chances


what does dilated cardiomyopathy result from?

extensively damaged myocardium muscle fibers


when do the cardiovascular components begin to function?

as early as about 4 weeks gestation and they function until the end of life